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Macrophage expression of activation markers in iron deficient conditions (1034.18)
Author(s) -
Leon Davila Minerva,
Contreras Irazú,
GutierrezSanchez Rosa,
Estrada José
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1034.18
Subject(s) - cd86 , cd80 , major histocompatibility complex , biology , microbiology and biotechnology , iron deficiency , mhc class i , flow cytometry , immunology , antigen , t cell , immune system , medicine , cytotoxic t cell , cd40 , biochemistry , in vitro , anemia
Objective: To determine the expression of major histocompatibility complex (MHC) class I and II and costimulatory molecules (CD80/CD86) by macrophages from iron deficient mice. Methods: Two groups of BALB/c mice were established from gestation: control (standard diet, 100ppm iron) and iron deficient (iron deficient diet, 10ppm iron). At 21 days of age, pups were weaned and their spleens were dissected for mononuclear cell purification. Purified cells were stained with fluorochrome‐conjugated antibodies for the surface markers CD11b, CD45, F4.80, MHC‐I, MHC‐II, CD80 and CD86. Analysis of expression of these markers was performed by flow cytometry. Results: The percentage of positive cells for MHC‐I, CD80 and CD86 was higher in iron deficient mice compared to controls. In contrast, the percentage of positive cells for MHC‐I was lower in iron deficient mice. However, the number of cells expressing MHC‐I, CD80 and CD86 was higher in the iron deficient group, while the number of cells expressing MHC‐II was higher in the control group. The mean fluorescence intensity for all markers was higher in iron deficient mice. Conclusion: Iron deficiency increases the basal expression of cell surface markers of activation in splenic macrophages. These results may have important implications in the activation of leucocytes in basal conditions in iron deficient individuals.